Michael J. Petris
Professor of Biochemistry
Biochemistry,Molecular Microbiology & Immunology,
|BSc||University of Melbourne||Melbourne, Australia||Biochemistry/Genetics|
|PhD||University of Melbourne||Melbourne, Australia||Genetics|
Notable honors and service
- Organizer FASEB Conference on Trace Element Micronutrients, 2006
- Organizing Committee, 5th International Meeting on Copper Homeostasis and its Disorders, 2006
- Scientific Advisory Committee, Gordon Research Conference on Cell Biology of Metals, 2005
- 4th International Meeting on Copper Homeostasis and its Disorders, 2004
The micronutrient copper (Cu) is essential for several key enzymatic processes involved in energy generation, protection against reactive oxygen species, formation of blood vessels, immune function, and healthy functioning of the central nervous system. This nutrient is able to exist in two oxidation states Cu1+ and Cu2+, and participate in the generation of reactive oxygen species. A delicate balance of copper homeostasis must be maintained to provide sufficient levels of this nutrient, while preventing toxic build up.
Copper and Cancer
Recent evidence suggests that copper plays a key role in tumor growth because this metal is essential for blood vessel formation (angiogenesis). Drugs that bind copper may inhibit tumor growth by preventing angiogenesis.
Copper and Alzheimer’s disease
Copper has been shown to interact with the toxic beta-amyloid peptide, and is present in high concentrations in amyloid plaques within in the brains of Alzheimer’s disease patients. Whether this copper is function in a protective or detrimental capacity is unknown.
Our lab is interested in characterizing the copper homeostasis pathways in animal and cell culture models of microbial infection, tumor growth and Alzheimer’s disease, and how this essential nutrient contributes to these pathologies.
Peterson TS, Thebeau CN, Ajit D, Camden JM, Woods LT, Gibson Wood W, Petris MJ, Sun GY, Erb L, Weisman GA. P2Y2 Nucleotide Receptor Upregulation and Activation Mediates Neurite Extension in IL-1β-treated Mouse Primary Cortical Neurons. J Neurochem. 2013 Mar 30. doi: 10.1111/jnc.12252.
Wang Y, Zhu S, Hodgkinson V, Prohaska JR, Weisman GA, Gitlin JD, Petris MJ. Maternofetal and neonatal copper requirements revealed by enterocyte-specific deletion of the Menkes disease protein. Am J Physiol Gastrointest Liver Physiol. 2012 Dec 1;303(11):G1236-44. doi: 10.1152/ajpgi.00339.2012. Epub 2012 Oct 11.
Wang Y, Zhu S, Weisman GA, Gitlin JD, Petris MJ. Conditional knockout of the Menkes disease copper transporter demonstrates its critical role in embryogenesis. PLoS One. 2012;7(8):e43039. doi: 10.1371/journal.pone.0043039. Epub 2012 Aug 10.
Woods LT, Camden JM, Batek JM, Petris MJ, Erb L, Weisman GA. P2X7 receptor activation induces inflammatory responses in salivary gland epithelium. Am J Physiol Cell Physiol. 2012 Oct 1;303(7):C790-801. doi: 10.1152/ajpcell.00072.2012. Epub 2012 Aug 8.
Hodgkinson V, Petris MJ. Copper homeostasis at the host-pathogen interface. J Biol Chem. 2012 Apr 20;287(17):13549-55. doi: 10.1074/jbc.R111.316406. Epub 2012 Mar 2. Review.
Research areas: Regulation of metal nutrition and impacts on common human diseases.
How to apply:
Electronic submission is encouraged, e-mail to firstname.lastname@example.org
Applicants should send CV and names of two references to:
Dr. Michael J. Petris
Christopher S. Bond Life Sciences Center
540D Bond Life Sciences Center
University of Missouri
Columbia, MO 65211